Immune modulation by fish kinetoplastid parasites: a role for nitric oxide

• Published in: Parasitology 2002-01, Vol.124 (1), p.77-86
• Main Authors: SAEIJ, J. P. J., VAN MUISWINKEL, W. B., GROENEVELD, A., WIEGERTJES, G. F.
• Format: Article
• Language: English
• Subjects: aminoguanidine; Animal aquaculture; Animal productions; Animals; Biological and medical sciences; Carps; Celbiologie en Immunologie; Cell Biology and Immunology; Cell Division - physiology; Cyprinus carpio; Enzyme Inhibitors - pharmacology; fish; Fish Diseases - immunology; Fish Diseases - parasitology; Fish parasites; Freshwater; Fundamental and applied biological sciences. Psychology; Guanidines - pharmacology; immunosuppression; Leerstoelgroep Celbiologie en immunologie; nitrate; Nitrates - metabolism; Nitric oxide; Nitric Oxide - biosynthesis; Nitric Oxide - immunology; Nitric Oxide Donors - pharmacology; Nitric Oxide Synthase - antagonists & inhibitors; Nitric Oxide Synthase Type II; nitric-oxide synthase inhibitor; nitric-oxide synthase inhibitors; Nitrites - metabolism; omega-N-Methylarginine - pharmacology; parasite; Phagocytosis; Pisciculture; S-Nitroso-N-Acetylpenicillamine - pharmacology; Survival; Trypanoplasma; Trypanoplasma borreli; Trypanosoma; Trypanosoma - growth & development; Trypanosoma - immunology; Trypanosoma carassii; Vertebrate aquaculture; WIAS
• ISSN: 0031-1820; 1469-8161
• DOI: 10.1017/S0031182001008915

Trypanoplasma borreli and Trypanosoma carassii are kinetoplastid parasites infecting cyprinid fish. We investigated the role of nitric oxide (NO) in immune modulation during T. borreli and T. carassii infection of carp. Phagocytic cells from different organs produced NO and serum nitrate levels increased, demonstrating that T. borreli activates NO production in vivo. In contrast, T. carassii did not induce NO production in vivo and inhibited LPS-induced NO production in vitro. Production of NO was detrimental to the host as T. borreli-infected carp treated with the inducible NO synthase inhibitor aminoguanidine had a higher survival than infected control carp. This detrimental effect can be explained (in part) by the toxicity of NO to cells in vitro as NO inhibited the proliferative response of blood and spleen leukocytes. Head-kidney phagocytes were resistant to the immunosuppressive effects of NO in vitro. The NO-inducing activity of T. borreli may be an adaptation developed to ensure survival and immune evasion in the fish host. Apparently, T. carassii has adopted another strategy by deactivating specific functions of phagocytes. Both strategies may ensure long-term survival of the parasite.